Enhancing chemotherapy response through augmented synthetic lethality by co-targeting nucleotide excision repair and cell-cycle checkpoints

Enhancing chemotherapy response through augmented synthetic lethality by co-targeting nucleotide excision repair and cell-cycle checkpoints

Cell cycle checkpoint kinase, MK2, is in synthetic relationship with p53 in the DNA damage response to chemotherapeutic agents. Here, the authors report XPA as a third gene in which simultaneous targeting of MK2 and XPA further enhances sensitivity to cisplatin in p53-deficient tumours.

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Detalles Bibliográficos
Autores principales: Yi Wen Kong, Erik C. Dreaden, Sandra Morandell, Wen Zhou, Sanjeev S. Dhara, Ganapathy Sriram, Fred C. Lam, Jesse C. Patterson, Mohiuddin Quadir, Anh Dinh, Kevin E. Shopsowitz, Shohreh Varmeh, Ömer H. Yilmaz, Stephen J. Lippard, H. Christian Reinhardt, Michael T. Hemann, Paula T. Hammond, Michael B. Yaffe
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2020
Materias:
Science
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Acceso en línea:https://doaj.org/article/968af14e7f93410d8098ad17f0bc993d
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Sumario:Cell cycle checkpoint kinase, MK2, is in synthetic relationship with p53 in the DNA damage response to chemotherapeutic agents. Here, the authors report XPA as a third gene in which simultaneous targeting of MK2 and XPA further enhances sensitivity to cisplatin in p53-deficient tumours.

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